A dysrhythmia is an abnormal heart beat pattern. One example of dysrhythmia is bradycardia wherein the heart beats at an abnormally slow rate or wherein significant pauses occur between consecutive beats. Other examples of dysrhythmias include tachyarrhythmias wherein the heart beats at an abnormally fast rate. With atrial tachycardia, such as atrial fibrillation (AF), the atria of the heart beat abnormally fast. With ventricular tachycardia, the ventricles of the heart beat abnormally fast. Though often unpleasant for the patient, a tachycardia is typically not fatal. However, some tachycardias, particularly ventricular tachycardia, can trigger ventricular fibrillation wherein the heart beats chaotically such that there is little or no net flow of blood from the heart to the brain and other organs. Ventricular tachycardia, if not terminated, is fatal. Hence, it is highly desirable to prevent or terminate dysrhythmias, particularly ventricular tachycardias.
One technique for preventing or terminating dysrhythmias is to overdrive pace the heart wherein a implantable cardiac stimulation device, such as a pacemaker or implantable cardioverter defibrillator (ICD), applies electrical pacing pulses to the heart at a rate somewhat faster than the intrinsic heart rate of the patient. For bradycardia, the cardiac stimulation device may be programmed to artificially pace the heart at a rate of 60 to 80 pulses per minute (ppm) to thereby prevent the heart from beating too slow and to eliminate any long pauses between heart beats. To prevent tachyarrhythmias from occurring, the cardiac stimulation device artificially paces the heart at a rate of at least five to ten beats per minute faster than the intrinsic tachyarrhythmia heart rate of the patient. In other words, a slight artificial tachycardia is induced and maintained in an effort to prevent an actual tachycardia from arising. If an actual tachycardia occurs, such as a supraventricular tachycardia (SVT) wherein the heart may begin beating suddenly at 150 beats per minute (bpm) or more, the cardiac stimulation device senses tachycardia and immediately begins pacing at a rate of at least five to ten ppm faster than the tachycardia, then slowly decreases the pacing rate in an effort to slowly reduce the heart rate back to a normal resting rate thereby terminating the tachycardia.
It is believed that overdrive pacing is effective for at least some patients for preventing or terminating the onset of an actual tachycardia for the following reasons. A normal, healthy heart beats only in response to electrical pulses generated from a portion of the heart referred to as the sinus node. The sinus node pulses are conducted to the various atria and ventricles of the heart via certain, normal conduction pathways. In some patients, however, additional portions of the heart also generate electrical pulses referred to as “ectopic” pulses. Each pulse, whether a sinus node pulse or an ectopic pulse has a refractory period subsequent thereto during which time the heart tissue is not responsive to any electrical pulses. A combination of sinus pulses and ectopic pulses can result in a dispersion of the refractory periods which, in turn, can trigger a tachycardia. By overdrive pacing the heart at a uniform rate, the likelihood of the occurrence of ectopic pulses is reduced and the refractory periods within the heart tissue are rendered uniform and periodic. Thus, the dispersion of refractory periods is reduced and tachycardias triggered thereby are substantially avoided. If a tachycardia nevertheless occurs, overdrive pacing at a rate faster than a tachycardia helps to eliminate ectopic pulses and reduce refractory period dispersion, and thereby helps to terminate the tachycardia.
Thus, it is desirable within patients prone to tachyarrhythmias to ensure that most beats of the heart are paced beats, as any unpaced beats may be ectopic beats. A high percentage of paced beats can be achieved simply by establishing a high overdrive pacing rate. However, a high overdrive pacing rate has disadvantages as well. For example, a high overdrive pacing rate may be unpleasant to the patient, particularly if the artificially-induced heart rate is relatively high in comparison with the heart rate that would otherwise normally occur. A high heart rate may also cause possible damage to the heart or may possibly trigger more serious dysrhythmias, such as a ventricular fibrillation.
A high overdrive rate may be especially problematic in patients suffering from heart failure, particularly if the heart failure is due to an impaired diastolic function. A high overdrive rate may actually exacerbate heart failure in these patients. Also, a high overdrive rate may be a problem in patients with coronary artery disease because increasing the heart rate decreases diastolic time and decreases perfusion, thus intensifying ischemia. Also, the need to apply overdrive pacing pulses operates to deplete a power supply of the implantable cardiac stimulation device, perhaps requiring frequent surgical replacement of the power supply.
Problems associated with overdrive pacing are particular severe for certain aggressive overdrive techniques which trigger an increase in the pacing rate based upon detection of a single intrinsic heart beat. With such techniques, a significant increase in the pacing rate is triggered by detection of a single intrinsic heart beat so as to respond promptly to the occurrence of a high rate tachycardia, such as an SVT. As a result, even in circumstances where a high rate tachycardia has not occurred, the detection of a single intrinsic heart beat can cause a significant increase in the overdrive rate, which may be reduced only gradually. If a second intrinsic heart beat is detected before the overdrive rate has been gradually lowered to a standard overdrive pacing rate, a still further increase in the pacing rate occurs. As can be appreciated, the foregoing can cause the overdrive pacing rate to increase significantly, perhaps to 150 ppm or more, even though no high rate tachycardia has occurred.
Hence, it would be desirable to provide techniques for overdrive pacing which reduce the average overdrive pacing rate, yet still attain a sufficiently high rate to significantly reduce the likelihood of a dysrhythmia within the patient or to terminate a dysrhythmia if one nevertheless occurs. In particular, it would be highly desirable to provide overdrive pacing techniques which permit a certain percentage of paced beats (such as 90% or 95%) to be sustained by the cardiac stimulation device so as to enable the overdrive rate to be minimized while still ensuring that most beats of the heart are paced beats. It was to these ends that aspects of the invention of the parent application were primarily directed.
The parent patent application referenced above was primarily directed to a technique for overdrive pacing the atria wherein an increase in the overdrive pacing rate is performed only in response to detection of at least two intrinsic atrial beats within a predetermined search period. In one specific technique, an increase in the atrial pacing rate occurs only if two P-waves are detected within X cardiac cycles of one another. In another specific technique, the overdrive rate is increased only if at least two P-waves are detected within a block of N consecutive cardiac cycles. In both techniques, the overdrive rate is decreased if no increase has occurred in the last Z cardiac cycles. By increasing the overdrive pacing rate only in response to detection of at least two P-waves within a predetermined number of cardiac cycles, an excessively high overdrive pacing rate is avoided which might otherwise occur if a rate increase were triggered based upon detection only of a single P-wave.
Insofar as the ventricles are concerned, overdrive pacing is also beneficial. However, unlike the atria, where it is generally desirable to achieve a high percentage of overdrive paced beats, with the ventricles it is generally best to provide rate smoothing, i.e. to provide a generally uniform ventricular rate as a function of time. Significant variations in the ventricular rate as a function of time presents a considerable annoyance to the patient who feels his or her heart rate increasing or decreasing frequently. Moreover, significant variations in ventricular rate can sometimes trigger atrial and ventricular tachyarrhythmias.
Various techniques have been developed in an attempt to provide rate smoothing of the ventricular rate. However, heretofore, ventricular rate smoothing techniques have often attempted to achieve rate smoothing primarily through fixed, non-overdrive ventricular pacing. In this regard, it has been found that there is a correlation between the degree of variation in the actual ventricular rate and the fixed rate at which the ventricles are paced. If the ventricles are paced at, for example, a fixed rate of 80 ppm, the resulting ventricular rate varies between the fixed rate of 80 ppm and much higher rates, such as 140 ppm. However, by pacing the ventricles at a higher fixed rate, for example, 100 ppm, the actual ventricular rate may only vary between the fixed rate of 100 ppm and a reduced upper rate of, perhaps, only 130 ppm. By pacing the ventricles at a still higher fixed rate, for example, 120 ppm, the actual ventricular rate may vary only within a much narrower range, such as from 120 to 125 ppm. In other words, the higher the fixed ventricular paced rate, the smoother the resulting ventricular rate.
Thus, rate smoothing of the ventricles can be achieved by pacing the ventricles at a high fixed rate. However, fixed rate pacing of the ventricles can result in “pacemaker syndrome”, which is typically characterized by hypotension, shortness of breath, and fatigue. Also, in many cases, fixed rate pacing of the ventricles at a high rate can cause “concealed retrograde conduction”, wherein a retrograde impulse travels from the ventricular pacing site back to the AV junction. Although this may not cause the atria to fire, the result is a lengthening of the AV junctional repolarization time, possibly adversely affecting the proper function of the atria and triggering atrial tachycardias.
Certain other ventricular rate smoothing techniques seek to achieve smoothing using adjustable ventricular pacing rates. However, these techniques appear to suffer from problems similar to those described above in connection with conventional atrial overdrive techniques, namely such techniques may be too sensitive to changes in the intrinsic ventricular rate. As an example of a technique which seeks to achieve ventricular rate smoothing using adjustable ventricular pacing rates see U.S. Pat. No. 5,792,193 to Stoop, entitled “Pacemaker System And A Method With Ventricular Rate Smoothing During High Rate Atrial Arrhythmia.” In the technique described by Stoop, during a pathologically high atrial rate episode, the pacemaker determines a ventricular pacing escape interval, corresponding to a flywheel rate, with the flywheel rate set at the beginning of the episode to be substantially equal to the atrial rate just before the high rate episode. As long as the episode continues, the flywheel rate is incremented upward whenever a ventricular sense occurs, thereby attempting to follow the average ventricular rate. Whenever a flywheel escape interval times out and a ventricular pacing pulse is delivered, flywheel rate is decremented. Ventricular sensing and pacing occurs only after timeout of the flywheel escape interval. Thus, detection of a single ventricular intrinsic sensed event causes an increase in the flywheel rate; whereas failure to detect an intrinsic ventricular event during the flywheel escape interval triggers an immediate decrease in the flywheel rate. As such, the pacemaker may be too sensitive to individual ventricular intrinsic sensed beats to provide for optimal ventricular rate smoothing. Moreover, the technique of Stoop only appears to provide for rate smoothing during episodes of pathologically high atrial rates and does not provide rate smoothing at other times.
In any case, it does not appear that, heretofore, any techniques have been developed for performing ventricular overdrive pacing, either for the purpose of achieving ventricular rate smoothing or for other reasons, which effectively controls and limits changes in the ventricular overdrive rate. Hence, it would be desirable to provide techniques for providing dynamic overdrive pacing of the ventricles either for ventricular rate smoothing or for other reasons, and aspects of the present CIP application are primarily directed to that end. Whereas atrial overdrive pacing is typically performed more or less continuously once activated by a physician, with ventricular overdrive pacing, care should be taken to ensure that the overdrive pacing of the ventricles is performed only when needed so as not to unduly increase the risk of ventricular dysrhythmias. Accordingly, techniques are also provided herein for activating and deactivating ventricular overdrive pacing based on various factors such as the capabilities of the particular pacing device (i.e. DDD vs. VVI pacers), the mode of operation (i.e. tracking vs. non-tracking mode) and the general medical condition of the patient (i.e. chronic AF vs. non-chronic AF.) In particular, techniques are provided for evaluating of the density of premature ventricular contractions (PVCs) and for disabling ventricular overdrive pacing in circumstances where overdrive pacing inadvertently triggers an increase in PVC density, which can in turn trigger ventricular tachyarrhythmia.